Break at 21D falls within the large intron of ds. Predicted product will be a secreted and truncated protein.
axon & larval optic lobe
costal vein | ectopic (with ds38k)
glial cell & larval optic lobe
humeral sclerite | ectopic (with ds38k)
wing hinge (with ds38k)
wing hinge | posterior (with ds38k)
wing margin | anterior | ectopic (with ds38k)
ds33k/Df(2L)Exel8003 stage 16 embryos have longer dorsal trunks than normal.
Scaffold axons project aberrantly in the larval optic lobes if ds33k mutants. Glia line these aberrant pathways and accumulate in abnormal destinations such as the lobula cortex.
Occasionally in ds38k/ds33k escapers (3 out of 72 heminota scored), the wing is replaced by a winglet and, posterior to it, a lateral protuberance that looks like an scutum and scutellum. The winglet is composed of proximal anterior structures arranged in a mirror-image duplication. The smallest examples of these winglets consist of a mirror image duplication of anterior hinge structures - the tegula and humeral sclerite. Larger examples also have a rudimentary wing blade consisting of a mirror image duplication of anterior structures - the costa and anterior wing margin.
ds33k/dsUAO71 flies have reduced viability, with only approximately half the expected number of adults emerging. Most of the adults that emerge quickly get stuck in the food and die. These flies also have a severely distorted body shape. ds33k/dsUAO71 flies have a wing tissue polarity phenotype similar to that of dsUAO71 homozygotes and hemizygotes. There is a region at the anterior margin with a swirl of partially reversed polarity hairs. In the anterior/central proximal part of the wing blade there are regions of completely reversed polarity (hairs pointing proximally). These regions are separated from regions of relatively normal polarity by a region of swirling. The polarity disruptions are more severe on the ventral surface of the wing than the dorsal surface. Prehairs initiate in the vicinity of the distal vertex of the wing cells (as in wild-type) in wing regions of ds33k/dsUAO71 flies that do not show substantial polarity alterations. In most regions with abnormal polarity, prehairs initiate at an alternative location along the cell periphery. In the regions with reversed polarity, prehairs initiate at the proximal-most vertex, while in regions where hair polarity is close to random and in the regions at the centre of swirls, prehairs initiate in the central regions of the cells. Approximately half the wings of ds33k/ds1 flies have a very weak tissue polarity phenotype, consisting of a couple of multiple hair cells and/or a small region of polarity disruption in the proximal part of the wing.
In addition to 100% penetrant defects in leg, wing and thorax, rough patches in the eye appear at low frequency. Anterior crossvein is displaced posteriorly. Combinations of ds33k and ds55 with each other or with Df(2L)S2 or Df(2L)ast1 eclose with very low frequency and show very strong deformations of thorax, legs and wings. Imaginal discs of dsM213/dsM213 or dsM213/ds33k are within the size range of normal discs, showing no tendency to overgrowth.
ds33k/+ has phenotype like dsW/+; scutellar bristles wide apart; wings shorter and wider than normal; crossveins close together. ds33k/dsW has extreme phenotype like dsd. RK3A. ds33k has not been separated from the recessive lethal factor of In(2LR)bwV1 and, therefore, has not been observed in homozygous condition.
ds33k/ds1 is an enhancer of phenotype of fzunspecified
ds33k is an enhancer of phenotype of fzunspecified
The distinctive ds polarity phenotype of ds33k/dsUAO71 flies (regions of reversed polarity on the wing) is suppressed by expression of fzI.hs 24 hours after white prepupa formation using a 1 hour heat shock. The appendage shape abnormalities and wing vein placement abnormalities are not suppressed. The fraction of the wing that shows abnormal polarity in fz24 flies is increased if the fly also carries ds1/ds33k. The domineering nonautonomy of fz1 clones is enhanced by dsUAO71/ds33k.
Bridges, 28th Nov. 1933.
Bridges.
Analysis of ds33k/dsUAO71 clones shows that ds displays domineering cell nonautonomy.
Strong allele.